New Elliptic Curve Record
The AI system Claude helped discover an elliptic curve with 30 independent points, surpassing the previous record of 29. On August 20, the online registry of elliptic curves ICARM added entry #273, which features this new curve with 30 rational points and a lower bound of its rank equal to 30.
The curve's equation and the coordinates of all 30 points are published on the entry page. ICARM verifies that each point lies on the curve and confirms their independence using an exact 2-descent calculation. The previous record, set in 2024, had 29 independent points, but the new entry contains a new equation and a new list of 30 points, increasing the known lower bound from 29 to 30.
The participants in the discovery, including Claude, Levent Alpöge, and Ava Howell, are credited in the entry comment. The result can be verified using the published equation and list of points, as described in the ICARM registry.
🔗 Read original →
The AI system Claude helped discover an elliptic curve with 30 independent points, surpassing the previous record of 29. On August 20, the online registry of elliptic curves ICARM added entry #273, which features this new curve with 30 rational points and a lower bound of its rank equal to 30.
The curve's equation and the coordinates of all 30 points are published on the entry page. ICARM verifies that each point lies on the curve and confirms their independence using an exact 2-descent calculation. The previous record, set in 2024, had 29 independent points, but the new entry contains a new equation and a new list of 30 points, increasing the known lower bound from 29 to 30.
The participants in the discovery, including Claude, Levent Alpöge, and Ava Howell, are credited in the entry comment. The result can be verified using the published equation and list of points, as described in the ICARM registry.
🔗 Read original →
web.math.pmf.unizg.hr
History of elliptic curves rank records
Table of elliptic curve rank records
SecureBio Detection Grant
The OpenAI Foundation has awarded SecureBio Detection $17.2 million to reduce the time from sample collection to early warning of a new pathogen from 14 to 3 days. On August 20, SecureBio Detection announced the grant, which will be used to reduce the time to result over the next year, add three cities to the nasal swab program, and increase sequencing volume.
SecureBio's approach involves collecting wastewater and nasal swabs, reading a wide range of DNA and RNA, and then searching for signs of an unusual pathogen. This method, known as metagenomic sequencing, allows for the detection of threats that are not yet on the list of known infections. The grant is focused on this stage of protection, which includes the entire process from sample collection to actionable result.
SecureBio plans to accelerate sample transportation, automate and parallelize sample preparation, and configure data processing to tap into more computing power for short periods. The average weekly volume is expected to grow to 80 billion read pairs, with each pair representing a short segment of genetic material read from both sides. The program began in 2021 as the Nucleic Acid Observatory project at the Sculpting Evolution group at the Massachusetts Institute of Technology. SecureBio will test the sensitivity of the entire chain from sample to final signal to different classes of viruses, and employees and external consultants will seek vulnerabilities that an attacker could exploit, as described in Nature Aging, July 2026.
🔗 Read original →
The OpenAI Foundation has awarded SecureBio Detection $17.2 million to reduce the time from sample collection to early warning of a new pathogen from 14 to 3 days. On August 20, SecureBio Detection announced the grant, which will be used to reduce the time to result over the next year, add three cities to the nasal swab program, and increase sequencing volume.
SecureBio's approach involves collecting wastewater and nasal swabs, reading a wide range of DNA and RNA, and then searching for signs of an unusual pathogen. This method, known as metagenomic sequencing, allows for the detection of threats that are not yet on the list of known infections. The grant is focused on this stage of protection, which includes the entire process from sample collection to actionable result.
SecureBio plans to accelerate sample transportation, automate and parallelize sample preparation, and configure data processing to tap into more computing power for short periods. The average weekly volume is expected to grow to 80 billion read pairs, with each pair representing a short segment of genetic material read from both sides. The program began in 2021 as the Nucleic Acid Observatory project at the Sculpting Evolution group at the Massachusetts Institute of Technology. SecureBio will test the sensitivity of the entire chain from sample to final signal to different classes of viruses, and employees and external consultants will seek vulnerabilities that an attacker could exploit, as described in Nature Aging, July 2026.
🔗 Read original →
PubMed Central (PMC)
Comparison of metagenomic and targeted methods for sequencing human pathogenic viruses from wastewater
Wastewater-based epidemiology is a powerful tool for monitoring the emergence and spread of viral pathogens at the population scale. Typical polymerase chain reaction (PCR)-based methods of quantitative and genomic monitoring of viruses in ...
France Allows Euthanasia
The French government has introduced a law that allows citizens to request assistance in dying under certain conditions. On August 18, President Emmanuel Macron signed law № 2026-794, which was published on August 19. This law adds the right to assisted death to the French Public Health Code, allowing adults to request assistance in dying if they have a severe, incurable illness that meets established criteria.
The law outlines a procedure for accessing assisted death, which requires five conditions to be met: the person must be at least 18 years old, a French citizen or a legal resident, have a severe, incurable illness that is advanced or terminal, experience suffering related to the illness that is unbearable or cannot be alleviated, and be able to express their free and informed will. A doctor informs the person about their condition, treatment options, palliative care, and available psychological support, after which the person can formalize their request.
A medical team, including the person's doctor, a specialist, and a medical worker from the treatment team, evaluates the illness, suffering, and free will. The team's decision is made by the first doctor, who must make a decision within 15 days of the request. After a positive decision, there is a waiting period of at least two days, during which the person must confirm their request. The law also establishes a commission to monitor the procedures and ensure that conditions and rules are respected, as reported in Le Monde, August 2026.
🔗 Read original →
The French government has introduced a law that allows citizens to request assistance in dying under certain conditions. On August 18, President Emmanuel Macron signed law № 2026-794, which was published on August 19. This law adds the right to assisted death to the French Public Health Code, allowing adults to request assistance in dying if they have a severe, incurable illness that meets established criteria.
The law outlines a procedure for accessing assisted death, which requires five conditions to be met: the person must be at least 18 years old, a French citizen or a legal resident, have a severe, incurable illness that is advanced or terminal, experience suffering related to the illness that is unbearable or cannot be alleviated, and be able to express their free and informed will. A doctor informs the person about their condition, treatment options, palliative care, and available psychological support, after which the person can formalize their request.
A medical team, including the person's doctor, a specialist, and a medical worker from the treatment team, evaluates the illness, suffering, and free will. The team's decision is made by the first doctor, who must make a decision within 15 days of the request. After a positive decision, there is a waiting period of at least two days, during which the person must confirm their request. The law also establishes a commission to monitor the procedures and ensure that conditions and rules are respected, as reported in Le Monde, August 2026.
🔗 Read original →
France Allows Assisted Death
The French government has introduced a law that allows citizens to request assistance in dying under certain conditions. On 18 August, President Emmanuel Macron signed law 2026-794, which was published on 19 August. This law adds the right to assisted death to the French Public Health Code, allowing adults to request assistance in dying if they have a severe, incurable illness.
The law outlines a procedure for accessing assisted death, which includes five conditions: the person must be at least 18 years old, a French citizen or a legal resident, have a severe incurable illness that is advanced or terminal, experience suffering that is unbearable and cannot be relieved, and be able to express their free and informed will. A doctor informs the person about their condition, treatment options, palliative care, and psychological support, after which the person can formalize their request.
A college of doctors, including the person's attending physician, a specialist, and a medical worker from the treatment team, evaluates the person's condition, suffering, and free will. The college helps establish the medical conditions, and the attending physician makes the decision, which must be made within 15 days of the request. After a positive decision, the person must wait at least 2 days before confirming their request, and on the day of the procedure, the doctor or nurse verifies the person's confirmation and ensures that they are not being pressured. The law also requires a commission to review each procedure to ensure that the conditions and rules are being followed, as reported in Le Monde, August 2026.
🔗 Read original →
The French government has introduced a law that allows citizens to request assistance in dying under certain conditions. On 18 August, President Emmanuel Macron signed law 2026-794, which was published on 19 August. This law adds the right to assisted death to the French Public Health Code, allowing adults to request assistance in dying if they have a severe, incurable illness.
The law outlines a procedure for accessing assisted death, which includes five conditions: the person must be at least 18 years old, a French citizen or a legal resident, have a severe incurable illness that is advanced or terminal, experience suffering that is unbearable and cannot be relieved, and be able to express their free and informed will. A doctor informs the person about their condition, treatment options, palliative care, and psychological support, after which the person can formalize their request.
A college of doctors, including the person's attending physician, a specialist, and a medical worker from the treatment team, evaluates the person's condition, suffering, and free will. The college helps establish the medical conditions, and the attending physician makes the decision, which must be made within 15 days of the request. After a positive decision, the person must wait at least 2 days before confirming their request, and on the day of the procedure, the doctor or nurse verifies the person's confirmation and ensures that they are not being pressured. The law also requires a commission to review each procedure to ensure that the conditions and rules are being followed, as reported in Le Monde, August 2026.
🔗 Read original →
DAXX Protein Role
The DAXX protein keeps virus-like DNA repeats switched off in microglia, the immune cells of the brain. Removing it causes inflammation and signs of cellular aging. On August 17, a study was published in Nature Neuroscience, where authors conditionally deleted the Daxx gene in adult mice and tracked the cells.
They studied how DNA packaging and microglia state changed as a result. In mammalian DNA, there are preserved repetitive fragments of ancient retroviruses. The cell usually keeps them switched off by tightly packaging DNA. In microglia, DAXX is the protein responsible for suppressing these virus-like repeats.
The level of DAXX decreased with age in both the brain and isolated microglia of mice. In human blood, higher DAXX gene activity was associated with lower activity of almost all studied types of retroelements. To establish the sequence of events, researchers deleted Daxx in young adult mice.
LTR-retroelements, one type of virus-like DNA repeat, were activated within the first few days. On some of these regions, the H3K9me3 chemical mark, which helps to tightly package DNA, was reduced. Then, microglia activated the interferon program and other inflammatory genes.
Cells lost signs of a calm state, and damage appeared in their DNA. Later, the number of microglial cells decreased, and among the remaining cells, some appeared with signs of senescence, a state in which a cell changes its function for an extended period.
🔗 Read original →
The DAXX protein keeps virus-like DNA repeats switched off in microglia, the immune cells of the brain. Removing it causes inflammation and signs of cellular aging. On August 17, a study was published in Nature Neuroscience, where authors conditionally deleted the Daxx gene in adult mice and tracked the cells.
They studied how DNA packaging and microglia state changed as a result. In mammalian DNA, there are preserved repetitive fragments of ancient retroviruses. The cell usually keeps them switched off by tightly packaging DNA. In microglia, DAXX is the protein responsible for suppressing these virus-like repeats.
The level of DAXX decreased with age in both the brain and isolated microglia of mice. In human blood, higher DAXX gene activity was associated with lower activity of almost all studied types of retroelements. To establish the sequence of events, researchers deleted Daxx in young adult mice.
LTR-retroelements, one type of virus-like DNA repeat, were activated within the first few days. On some of these regions, the H3K9me3 chemical mark, which helps to tightly package DNA, was reduced. Then, microglia activated the interferon program and other inflammatory genes.
Cells lost signs of a calm state, and damage appeared in their DNA. Later, the number of microglial cells decreased, and among the remaining cells, some appeared with signs of senescence, a state in which a cell changes its function for an extended period.
🔗 Read original →
Nature
Microglia activation by derepression of endogenous retroviruses drives inflammation and cellular senescence
Nature Neuroscience - Reawakening of endogenous retroviruses due to loss of chromatin compaction causes microglia to acquire aging-associated features, leading to perturbed tissue homeostasis and...
DAXX Protein Role
The DAXX protein keeps virus-like DNA repeats switched off in microglia, the immune cells of the brain, and its removal causes inflammation and signs of cellular aging. On August 17, an article was published in Nature Neuroscience, where authors conditionally knocked out the Daxx gene in adult mice and tracked the cells, studying how DNA packaging and microglia state changed.
In mammalian DNA, repetitive fragments of ancient retroviruses are preserved, and cells usually keep them switched off by tightly packaging DNA. In microglia, DAXX is the protein responsible for suppressing these virus-like repeats. The level of DAXX decreased with age in both the brain and isolated microglia of mice. In human blood, higher DAXX gene activity was associated with lower activity of almost all studied types of retroelements.
To establish the sequence of events, researchers removed Daxx from young adult mice, and LTR-retroelements, one type of virus-like DNA repeat, were activated within the first few days. The chemical mark H3K9me3, which helps to tightly package DNA, was reduced on some of these regions. Then, microglia activated the interferon program and other inflammatory genes, and cells lost signs of a calm state, with damage appearing in their DNA.
Later, the number of microglial cells decreased, and among the remaining cells, some appeared with signs of senescence, a state in which a cell changes its work for an extended period. The authors separately checked the role of PML, a protein that supports this state, and found that when Daxx and Pml genes were simultaneously removed, there were fewer cells with positive laboratory tests for senescence and more microglial cells by the eighth week.
🔗 Read original →
The DAXX protein keeps virus-like DNA repeats switched off in microglia, the immune cells of the brain, and its removal causes inflammation and signs of cellular aging. On August 17, an article was published in Nature Neuroscience, where authors conditionally knocked out the Daxx gene in adult mice and tracked the cells, studying how DNA packaging and microglia state changed.
In mammalian DNA, repetitive fragments of ancient retroviruses are preserved, and cells usually keep them switched off by tightly packaging DNA. In microglia, DAXX is the protein responsible for suppressing these virus-like repeats. The level of DAXX decreased with age in both the brain and isolated microglia of mice. In human blood, higher DAXX gene activity was associated with lower activity of almost all studied types of retroelements.
To establish the sequence of events, researchers removed Daxx from young adult mice, and LTR-retroelements, one type of virus-like DNA repeat, were activated within the first few days. The chemical mark H3K9me3, which helps to tightly package DNA, was reduced on some of these regions. Then, microglia activated the interferon program and other inflammatory genes, and cells lost signs of a calm state, with damage appearing in their DNA.
Later, the number of microglial cells decreased, and among the remaining cells, some appeared with signs of senescence, a state in which a cell changes its work for an extended period. The authors separately checked the role of PML, a protein that supports this state, and found that when Daxx and Pml genes were simultaneously removed, there were fewer cells with positive laboratory tests for senescence and more microglial cells by the eighth week.
🔗 Read original →
Nature
Microglia activation by derepression of endogenous retroviruses drives inflammation and cellular senescence
Nature Neuroscience - Reawakening of endogenous retroviruses due to loss of chromatin compaction causes microglia to acquire aging-associated features, leading to perturbed tissue homeostasis and...
CoQ10 Trial in Elderly
The University Medical Centre Ljubljana has registered a 10-week trial of coenzyme Q10 in people over 65 with early signs of frailty. One hundred participants will receive either 200mg of coenzyme Q10 or a placebo daily for ten weeks. The primary outcome measure will be GDF-15, a protein that indicates cellular and mitochondrial stress.
The study will also include people with low physical function test results or high vulnerability scores. Coenzyme Q10 plays a role in the functioning of mitochondria, the cellular structures where nutrients are converted into energy. Researchers will check one chain at several levels: CoQ10 concentration in plasma will show if the supplement reached the bloodstream; GDF-15 will provide a measurable signal of cellular stress; physical tests, grip strength, and frailty scales will allow comparison of this signal with how a person walks, gets up from a chair, and preserves strength.
The trial is scheduled to start in September 2026 and end in February 2027, as listed in the ClinicalTrials.gov registry.
🔗 Read original →
The University Medical Centre Ljubljana has registered a 10-week trial of coenzyme Q10 in people over 65 with early signs of frailty. One hundred participants will receive either 200mg of coenzyme Q10 or a placebo daily for ten weeks. The primary outcome measure will be GDF-15, a protein that indicates cellular and mitochondrial stress.
The study will also include people with low physical function test results or high vulnerability scores. Coenzyme Q10 plays a role in the functioning of mitochondria, the cellular structures where nutrients are converted into energy. Researchers will check one chain at several levels: CoQ10 concentration in plasma will show if the supplement reached the bloodstream; GDF-15 will provide a measurable signal of cellular stress; physical tests, grip strength, and frailty scales will allow comparison of this signal with how a person walks, gets up from a chair, and preserves strength.
The trial is scheduled to start in September 2026 and end in February 2027, as listed in the ClinicalTrials.gov registry.
🔗 Read original →
PubMed Central (PMC)
Effect of Ubiquinol on Cognitive Function, Blood Pressure, Arterial Stiffness, and Biomarkers of Oxidative Stress and Inflammation…
Older age is typically characterized by decrements in cognitive performance relative to younger adults, though it may not necessarily reach clinical impairment. Dietary supplementation with ubiquinol, the reduced form of the antioxidant and cellular ...
AI Drug Search
Patrick Maloone proposed evaluating AI-powered drug searches by selecting candidates for laboratory testing on August 20. In his model, scientists guide multiple specialized programs that narrow down thousands of protein or molecule variants to a short list for laboratory testing. The model can suggest many plausible protein or molecule variants, but the laboratory can only synthesize and test a small fraction.
Maloone's approach is based on the recent Claude campaign, which designed miniproteins. The agent selected a protein segment, design programs, and candidate lists, and two laboratories then tested whether they bound to the target protein. Many decisions need to be made between the model's request and the experimental result, and candidate selection is already a separate task. In a blind test of 511 antibodies in the second task, most AI participants performed worse than a basic strategy in selecting variants that bound to the target protein.
Laboratories need a list of candidates that are most likely to yield results in the next experiment. In Maloone's scenario, the scientist assigns programs to separate stages: literature search, modeling, design, result analysis, and experiment planning. The knowledge that usually remains in the specialist's head is proposed to be transformed into rules, examples, tools, and checks accessible to programs. To prioritize candidates, one needs to select a program for a specific question, distribute computations, implement control checks, preserve data provenance, and set evaluation rules. Then, one needs to troubleshoot failures, as described in Nature Aging, July 2026.
🔗 Read original →
Patrick Maloone proposed evaluating AI-powered drug searches by selecting candidates for laboratory testing on August 20. In his model, scientists guide multiple specialized programs that narrow down thousands of protein or molecule variants to a short list for laboratory testing. The model can suggest many plausible protein or molecule variants, but the laboratory can only synthesize and test a small fraction.
Maloone's approach is based on the recent Claude campaign, which designed miniproteins. The agent selected a protein segment, design programs, and candidate lists, and two laboratories then tested whether they bound to the target protein. Many decisions need to be made between the model's request and the experimental result, and candidate selection is already a separate task. In a blind test of 511 antibodies in the second task, most AI participants performed worse than a basic strategy in selecting variants that bound to the target protein.
Laboratories need a list of candidates that are most likely to yield results in the next experiment. In Maloone's scenario, the scientist assigns programs to separate stages: literature search, modeling, design, result analysis, and experiment planning. The knowledge that usually remains in the specialist's head is proposed to be transformed into rules, examples, tools, and checks accessible to programs. To prioritize candidates, one needs to select a program for a specific question, distribute computations, implement control checks, preserve data provenance, and set evaluation rules. Then, one needs to troubleshoot failures, as described in Nature Aging, July 2026.
🔗 Read original →
X (formerly Twitter)
Patrick Malone, MD PhD (@patricksmalone) on X
some thoughts on Claude’s protein design work, and implications for the future of AI drug discovery:
1. the optimal biotech company will get shockingly small. a couple great scientists will supervise hundreds of agents doing literature work, modeling, design…
1. the optimal biotech company will get shockingly small. a couple great scientists will supervise hundreds of agents doing literature work, modeling, design…
AI Drug Search
Patrick Maloone proposed evaluating AI-powered drug searches by selecting candidates for laboratory testing on August 20. In his post, Maloone described his AI-powered drug search model, where scientists guide multiple specialized programs to narrow down thousands of protein or molecule variants to a short list for laboratory testing.
The model can propose a large number of plausible protein or molecule variants, but the laboratory can only synthesize and test a small fraction of them. Maloone formulated this gap as: "100,000 plausible molecules are only useful when you can choose 20 that are worth testing". He drew inspiration from the recent Claude campaign on miniprotein design, where an agent selected a protein segment, design programs, and candidate lists, and two laboratories then tested whether they bound to the target protein.
In Maloone's scenario, a scientist assigns programs to individual stages: literature search, modeling, design, result analysis, and experiment planning. To prioritize candidates, one needs to select a program for a specific question, distribute computations, implement control checks, preserve data provenance, and set evaluation rules. Then, one needs to troubleshoot failures, as described in Nature Aging, July 2026.
🔗 Read original →
Patrick Maloone proposed evaluating AI-powered drug searches by selecting candidates for laboratory testing on August 20. In his post, Maloone described his AI-powered drug search model, where scientists guide multiple specialized programs to narrow down thousands of protein or molecule variants to a short list for laboratory testing.
The model can propose a large number of plausible protein or molecule variants, but the laboratory can only synthesize and test a small fraction of them. Maloone formulated this gap as: "100,000 plausible molecules are only useful when you can choose 20 that are worth testing". He drew inspiration from the recent Claude campaign on miniprotein design, where an agent selected a protein segment, design programs, and candidate lists, and two laboratories then tested whether they bound to the target protein.
In Maloone's scenario, a scientist assigns programs to individual stages: literature search, modeling, design, result analysis, and experiment planning. To prioritize candidates, one needs to select a program for a specific question, distribute computations, implement control checks, preserve data provenance, and set evaluation rules. Then, one needs to troubleshoot failures, as described in Nature Aging, July 2026.
🔗 Read original →
X (formerly Twitter)
Patrick Malone, MD PhD (@patricksmalone) on X
some thoughts on Claude’s protein design work, and implications for the future of AI drug discovery:
1. the optimal biotech company will get shockingly small. a couple great scientists will supervise hundreds of agents doing literature work, modeling, design…
1. the optimal biotech company will get shockingly small. a couple great scientists will supervise hundreds of agents doing literature work, modeling, design…
Hepatitis C Treatment Boost
The OpenAI Foundation will allocate $100 million to help patients with hepatitis C receive treatment. On August 13, the Common Health Coalition announced the Breakthroughs to Follow-Through (B2F) program, funded by the OpenAI Foundation. Over two years, B2F aims to at least double the number of people cured of hepatitis C in eight initial US states and local jurisdictions.
The first funds will go to local partnerships and NGOs in Alabama, Illinois, Louisiana, and Massachusetts. Hepatitis C is typically treated with antiviral tablets: the course takes 8–12 weeks. The US Centers for Disease Control and Prevention (CDC) report that these medications cure more than 95% of people with this infection. However, a person still needs to be diagnosed, see a doctor, complete the course, and confirm that the virus has disappeared.
The coalition estimates that in the US, about two out of three people with hepatitis C remain untreated. B2F will fund local partnerships, technical assistance, regional best practice sharing, and evaluation of patient treatment pathways. The funds will cover the path from diagnosis to confirmed cure. For AI, the release names three tasks: searching medical records for people who have fallen between diagnosis and treatment; preparing summaries for doctors and taking on routine administrative work; and showing teams where patients are most often lost. This should help local teams re-establish contact with patients and identify where treatment is interrupted, as described in the Nature Aging, July 2026 issue.
🔗 Read original →
The OpenAI Foundation will allocate $100 million to help patients with hepatitis C receive treatment. On August 13, the Common Health Coalition announced the Breakthroughs to Follow-Through (B2F) program, funded by the OpenAI Foundation. Over two years, B2F aims to at least double the number of people cured of hepatitis C in eight initial US states and local jurisdictions.
The first funds will go to local partnerships and NGOs in Alabama, Illinois, Louisiana, and Massachusetts. Hepatitis C is typically treated with antiviral tablets: the course takes 8–12 weeks. The US Centers for Disease Control and Prevention (CDC) report that these medications cure more than 95% of people with this infection. However, a person still needs to be diagnosed, see a doctor, complete the course, and confirm that the virus has disappeared.
The coalition estimates that in the US, about two out of three people with hepatitis C remain untreated. B2F will fund local partnerships, technical assistance, regional best practice sharing, and evaluation of patient treatment pathways. The funds will cover the path from diagnosis to confirmed cure. For AI, the release names three tasks: searching medical records for people who have fallen between diagnosis and treatment; preparing summaries for doctors and taking on routine administrative work; and showing teams where patients are most often lost. This should help local teams re-establish contact with patients and identify where treatment is interrupted, as described in the Nature Aging, July 2026 issue.
🔗 Read original →
Brain Computer Interface
The main idea is to consider the brain as a computational system, which means its functions can be studied and gradually replaced with artificial components. A key example is Prima, a neuroimplant for restoring vision in people with retinal degeneration. The system works through the remaining neural pathways of the eye, with a miniature chip implanted under the retina, containing 378 photoreceptive pixels.
The chip converts light into electrical impulses, stimulating retinal cells and sending information to the brain. In clinical trials, patients with severe central vision loss were able to perform tasks that were previously impossible, such as reading letters and words, and solving Sudoku and crosswords. However, the technology is still far from natural vision, with limited resolution and a small field of view.
According to Max Hodak, such technologies are the real future of neurointerfaces. He believes that attempts to create a "brain keyboard" that allows typing thoughts directly are overestimating the problem, citing an estimate of approximately 10 bits per second for the speed of information transmission from consciousness. A more promising direction is to restore damaged communication channels between the brain and body, such as vision, hearing, movement, and balance, as mentioned in the Nature Aging journal.
🔗 Read original →
The main idea is to consider the brain as a computational system, which means its functions can be studied and gradually replaced with artificial components. A key example is Prima, a neuroimplant for restoring vision in people with retinal degeneration. The system works through the remaining neural pathways of the eye, with a miniature chip implanted under the retina, containing 378 photoreceptive pixels.
The chip converts light into electrical impulses, stimulating retinal cells and sending information to the brain. In clinical trials, patients with severe central vision loss were able to perform tasks that were previously impossible, such as reading letters and words, and solving Sudoku and crosswords. However, the technology is still far from natural vision, with limited resolution and a small field of view.
According to Max Hodak, such technologies are the real future of neurointerfaces. He believes that attempts to create a "brain keyboard" that allows typing thoughts directly are overestimating the problem, citing an estimate of approximately 10 bits per second for the speed of information transmission from consciousness. A more promising direction is to restore damaged communication channels between the brain and body, such as vision, hearing, movement, and balance, as mentioned in the Nature Aging journal.
🔗 Read original →
YouTube
From Restoring Sight to Reimagining the Brain, with Max Hodak
Max Hodak, co-founder and CEO of Science Corporation, joins Sarah Guo to discuss the future of vision, brain-computer interfaces, and the human experience. Max explains how Science’s PRIMA retinal implant could restore functional vision for people who have…
Lab-Grown Spinal Cord
Scientists are set to implant the world's first "lab-grown" spinal cord segment. The procedure involves taking a standard blood sample from a patient and converting its cells into induced pluripotent stem cells (iPSC). These cells can become any type of tissue. They are then used to create a personalized neural implant - essentially a "biological spare part" - to replace a damaged spinal cord segment.
The implant is made from the patient's own cells, minimizing the risk of immune rejection and ensuring better integration with tissues than any donor or synthetic materials. Creating one such implant takes several months, so blood collection from potential patients is already underway to progress regulatory stages in parallel.
The first operation may take place in the first half of 2027, according to an official estimate by Matricelf, the technology developer, as reported in Nature Aging, July 2026.
🔗 Read original →
Scientists are set to implant the world's first "lab-grown" spinal cord segment. The procedure involves taking a standard blood sample from a patient and converting its cells into induced pluripotent stem cells (iPSC). These cells can become any type of tissue. They are then used to create a personalized neural implant - essentially a "biological spare part" - to replace a damaged spinal cord segment.
The implant is made from the patient's own cells, minimizing the risk of immune rejection and ensuring better integration with tissues than any donor or synthetic materials. Creating one such implant takes several months, so blood collection from potential patients is already underway to progress regulatory stages in parallel.
The first operation may take place in the first half of 2027, according to an official estimate by Matricelf, the technology developer, as reported in Nature Aging, July 2026.
🔗 Read original →
EurekAlert!
A step toward the world’s first implantation of an engineered spinal cord
Biotech company Matricelf and Loewenstein Rehabilitation Medical Center will collaborate in preparations for the world’s first implantation of an engineered spinal cord in a paralyzed patient. The scientific breakthrough is based on a revolutionary…
Electronic Skin
The new electronic skin can give people with prosthetics a partial sense of touch - pressure, temperature, and even surface texture. The entire system is 10 times more accurate than commercial sensors in modern robotic gloves. It consists of thin, multi-layered modules that contain pressure and temperature sensors, which work like human skin: they detect the slightest changes and transmit data in real time.
The main achievement is the ability to create skin of an individual shape that precisely replicates the curves of a specific prosthesis. This is done using the "scan-model-print" method: the prosthesis is first scanned, then a sensor map is applied to its geometry, and everything is printed in 3D. The sensors do not require glue - the modules simply snap together like constructor parts. The sensor density is high: the system covers flat and curved surfaces without "blind spots".
At the same time, production remains cheap - laser cutting and regular 3D printing are used. This makes electronic skin available for mass use, not just for expensive experimental prosthetics. In the future, developers want to add feedback so that a person can not only "collect data" but also really feel the touch. Researchers are already working on an actuator that will convert sensor signals into nerve stimulation near the amputation site, as described in Cell Reports Physical Science.
🔗 Read original →
The new electronic skin can give people with prosthetics a partial sense of touch - pressure, temperature, and even surface texture. The entire system is 10 times more accurate than commercial sensors in modern robotic gloves. It consists of thin, multi-layered modules that contain pressure and temperature sensors, which work like human skin: they detect the slightest changes and transmit data in real time.
The main achievement is the ability to create skin of an individual shape that precisely replicates the curves of a specific prosthesis. This is done using the "scan-model-print" method: the prosthesis is first scanned, then a sensor map is applied to its geometry, and everything is printed in 3D. The sensors do not require glue - the modules simply snap together like constructor parts. The sensor density is high: the system covers flat and curved surfaces without "blind spots".
At the same time, production remains cheap - laser cutting and regular 3D printing are used. This makes electronic skin available for mass use, not just for expensive experimental prosthetics. In the future, developers want to add feedback so that a person can not only "collect data" but also really feel the touch. Researchers are already working on an actuator that will convert sensor signals into nerve stimulation near the amputation site, as described in Cell Reports Physical Science.
🔗 Read original →
Cell Reports Physical Science
A geometry-aware and customizable multimodal sensing system for texture and material identification in prosthetics
Shen et al. present a customizable electronic skin that conforms to prosthetic surfaces
and combines pressure, temperature, and neural-network calibration. The modular system
maps tactile signals with high spatial resolution and enables material and texture…
and combines pressure, temperature, and neural-network calibration. The modular system
maps tactile signals with high spatial resolution and enables material and texture…
Matwings Reports Progress
Matwings announced that laboratory measurements helped select the next protein variants for the GenSci148 candidate. On August 20, the company reported on four cycles of GenSci148 development, a protein candidate for treating retinal diseases. AI suggested new protein variants, which were then tested in the laboratory, and the results were used to inform the next round of variant selection and property improvement.
The protein must not only bind to the target but also remain stable, be producible, and have a suitable solution for administration. Therefore, each laboratory round in this program answered two questions: which variants to develop further and which properties to test. In the August 20 release, Matwings wrote that over four rounds, the teams tested 222 protein variants: 92 in the first, 30 in the second, and 50 in both the third and fourth.
The first two rounds focused on biological activity, while the third and fourth rounds added viscosity of the concentrated solution and other necessary properties for development. The company reports that the results of each round informed the next iteration of design. Laboratory measurements immediately influenced two decisions: which set of protein variants to create and what requirements to impose on them. GenSci148 is a candidate for treating retinal diseases, and according to the GenSci page, the Chinese drug regulator has approved it for clinical trials for three such diseases, to which the four rounds reported by Matwings relate, as cited in company reports.
🔗 Read original →
Matwings announced that laboratory measurements helped select the next protein variants for the GenSci148 candidate. On August 20, the company reported on four cycles of GenSci148 development, a protein candidate for treating retinal diseases. AI suggested new protein variants, which were then tested in the laboratory, and the results were used to inform the next round of variant selection and property improvement.
The protein must not only bind to the target but also remain stable, be producible, and have a suitable solution for administration. Therefore, each laboratory round in this program answered two questions: which variants to develop further and which properties to test. In the August 20 release, Matwings wrote that over four rounds, the teams tested 222 protein variants: 92 in the first, 30 in the second, and 50 in both the third and fourth.
The first two rounds focused on biological activity, while the third and fourth rounds added viscosity of the concentrated solution and other necessary properties for development. The company reports that the results of each round informed the next iteration of design. Laboratory measurements immediately influenced two decisions: which set of protein variants to create and what requirements to impose on them. GenSci148 is a candidate for treating retinal diseases, and according to the GenSci page, the Chinese drug regulator has approved it for clinical trials for three such diseases, to which the four rounds reported by Matwings relate, as cited in company reports.
🔗 Read original →
PR Newswire
Matwings Demonstrates Closed-Loop Protein AI Through Four AI-Wet Lab Cycles and 222 Protein Variants
/PRNewswire/ -- Shanghai Matwings Technology Co., Ltd. ("Matwings") today announced that GenSci148 Injection, an investigational ophthalmic biologic developed...
Longevity Leaders
TIME magazine has released a collection of 12 profiles on aging biology, from cell reprogramming to human trials. The Longevity Leaders 2026 issue features individuals working to change, measure, and test age-related processes in cells and humans. The discovery by Sinyi Yamanaka led to cell reprogramming attempts to restore cells to a younger state.
The magazine includes David Sinclair and Juan Carlos Izpisua Belmonte, who are developing this research line. Nir Barzilai studies the genetic and biological characteristics of people who remain healthy after 95 years and is involved in the search for biomarkers - measurable signs of age-related changes.
Andrea Maier takes this question to human trials, often recruiting participants with a higher biological age than their calendar age. Steve Horvath's work helps select the group, and a planned randomized trial will test whether the intervention helps this group. The XPRIZE Healthspan competition adds a general way to compare different approaches, with finalists evaluating the effects of interventions on muscle, cognitive, and immune function, as cited in Nature Aging, July 2026.
🔗 Read original →
TIME magazine has released a collection of 12 profiles on aging biology, from cell reprogramming to human trials. The Longevity Leaders 2026 issue features individuals working to change, measure, and test age-related processes in cells and humans. The discovery by Sinyi Yamanaka led to cell reprogramming attempts to restore cells to a younger state.
The magazine includes David Sinclair and Juan Carlos Izpisua Belmonte, who are developing this research line. Nir Barzilai studies the genetic and biological characteristics of people who remain healthy after 95 years and is involved in the search for biomarkers - measurable signs of age-related changes.
Andrea Maier takes this question to human trials, often recruiting participants with a higher biological age than their calendar age. Steve Horvath's work helps select the group, and a planned randomized trial will test whether the intervention helps this group. The XPRIZE Healthspan competition adds a general way to compare different approaches, with finalists evaluating the effects of interventions on muscle, cognitive, and immune function, as cited in Nature Aging, July 2026.
🔗 Read original →
Nature
Anti-aging interventions need less hype and more clinical evidence
Nature Medicine - The aging field needs to develop reliable biomarkers of aging and a solid evidence base for the safety and efficacy of anti-aging treatments.
Telomere Protein Found
Researchers have discovered the telomere protein TRF2 on DNA fragments associated with inflammation in cells that have stopped dividing. In several models of human cells, scientists observed DNA fragments with TRF2 - a protein that protects telomeres, the ends of chromosomes - in the cytoplasm. These fragments showed signs of DNA damage and cGAS, a protein that recognizes DNA in the cytoplasm.
The nucleus normally keeps chromosomes inside the cell. When DNA enters the cytoplasm, cGAS perceives it as a danger signal and triggers an inflammatory response. In senescent cells, this response supports the SASP mode, in which the cell releases cytokines and other substances that change the environment around it. These experiments build on the work of Renuki Kandhaya-Pillai's group from 2017, which found that prolonged exposure to TNFα - an inflammatory signaling molecule - converted endothelial cells into senescence and maintained cytokine release through STAT proteins.
The new study asked what DNA might be the source of the cGAS signal in the same model. Researchers compared dividing cells with cells that had entered senescence due to repeated divisions or TNFα, as well as with fibroblasts from people with inherited premature aging syndromes or LMNA gene mutations. In these models, TRF2 was detected on cytoplasmic fragments near γH2AX - a protein marker of DNA damage. Prolonged TNFα treatment reduced the level of lamin B1, a nuclear envelope protein, and authors observed breaks in the envelope and the release of nuclear DNA into the cytoplasm.
🔗 Read original →
Researchers have discovered the telomere protein TRF2 on DNA fragments associated with inflammation in cells that have stopped dividing. In several models of human cells, scientists observed DNA fragments with TRF2 - a protein that protects telomeres, the ends of chromosomes - in the cytoplasm. These fragments showed signs of DNA damage and cGAS, a protein that recognizes DNA in the cytoplasm.
The nucleus normally keeps chromosomes inside the cell. When DNA enters the cytoplasm, cGAS perceives it as a danger signal and triggers an inflammatory response. In senescent cells, this response supports the SASP mode, in which the cell releases cytokines and other substances that change the environment around it. These experiments build on the work of Renuki Kandhaya-Pillai's group from 2017, which found that prolonged exposure to TNFα - an inflammatory signaling molecule - converted endothelial cells into senescence and maintained cytokine release through STAT proteins.
The new study asked what DNA might be the source of the cGAS signal in the same model. Researchers compared dividing cells with cells that had entered senescence due to repeated divisions or TNFα, as well as with fibroblasts from people with inherited premature aging syndromes or LMNA gene mutations. In these models, TRF2 was detected on cytoplasmic fragments near γH2AX - a protein marker of DNA damage. Prolonged TNFα treatment reduced the level of lamin B1, a nuclear envelope protein, and authors observed breaks in the envelope and the release of nuclear DNA into the cytoplasm.
🔗 Read original →
PubMed Central (PMC)
TRF2 enriched cytoplasmic chromatin drives cGAS-STAT1-mediated inflammation in senescence
Telomere dysfunction, persistent DNA damage, and chronic inflammation are interconnected hallmarks of cellular senescence, but their molecular links remains poorly defined. Here, we find that senescent cells accumulate telomeric protein ...
Longevity Study Results
A recent study published in Nature Medicine on August 21 analyzed 51 longevity studies with 3,128 blood samples. The authors calculated 16 epigenetic clocks, which are markers on DNA associated with age, mortality risk, or aging rate. Clinical outcomes of anti-aging interventions become apparent over years, as diseases and mortality develop slowly.
The researchers took blood samples before and after interventions and used the clocks as a rapid measure. They should notice changes and provide consistent results upon repeated measurements. The same group had previously shown that re-analyzing the same sample can be accurate, but a new sample from the same person can give a different result.
The authors collected pairs of samples before and after interventions from the TranslAGE database, unified participant information and observation periods, and recalculated the same panel of clocks for each sample. They separated the clock measurements from calendar age and compared the results for each person. This allowed them to determine which measures shifted after different interventions and in different participant groups. Measures developed to assess aging rate or mortality risk, such as DunedinPACE, more often provided a consistent response.
🔗 Read original →
A recent study published in Nature Medicine on August 21 analyzed 51 longevity studies with 3,128 blood samples. The authors calculated 16 epigenetic clocks, which are markers on DNA associated with age, mortality risk, or aging rate. Clinical outcomes of anti-aging interventions become apparent over years, as diseases and mortality develop slowly.
The researchers took blood samples before and after interventions and used the clocks as a rapid measure. They should notice changes and provide consistent results upon repeated measurements. The same group had previously shown that re-analyzing the same sample can be accurate, but a new sample from the same person can give a different result.
The authors collected pairs of samples before and after interventions from the TranslAGE database, unified participant information and observation periods, and recalculated the same panel of clocks for each sample. They separated the clock measurements from calendar age and compared the results for each person. This allowed them to determine which measures shifted after different interventions and in different participant groups. Measures developed to assess aging rate or mortality risk, such as DunedinPACE, more often provided a consistent response.
🔗 Read original →
Nature
Responsiveness of epigenetic aging biomarkers to longevity interventions in humans
Nature Medicine - The responsiveness of 16 different epigenetic aging clocks to a broad array of pharmacological and lifestyle interventions in humans was assessed across 51 different longitudinal...
IGF-1 Restores Brain Barrier
Researchers found that IGF-1 is a crucial factor in restoring the protective barrier of the brain in old mice with young circulation. In a study published on August 20, 2026, 18-month-old mice were surgically connected to 4.5-month-old mice through a shared circulatory system. The young circulation reduced leakage through the protective barrier between the blood and brain tissue and increased the density of small vessels.
When the level of IGF-1 was reduced in young mice, and its receptor was removed from the vascular wall of old mice, both improvements weakened. This experiment is called heterochronic parabiosis, where an old and young mouse are surgically connected to share a circulatory system. In a 2024 study, the same group found that old partners had a less permeable blood-brain barrier and a denser network of capillaries, the smallest vessels.
The new study checks which signal in the shared blood is involved in these changes. The authors chose IGF-1, a signaling protein whose level in the blood decreases with age. To respond to it, the protein must enter the shared circulation, and the inner lining of the vessel, the endothelium, must receive the signal through the IGF-1R receptor. The researchers evaluated the state of the barrier by introducing glowing molecules of different sizes into the blood and observing whether they exited the vessels into the brain tissue, as reported in Nature Aging, July 2026.
🔗 Read original →
Researchers found that IGF-1 is a crucial factor in restoring the protective barrier of the brain in old mice with young circulation. In a study published on August 20, 2026, 18-month-old mice were surgically connected to 4.5-month-old mice through a shared circulatory system. The young circulation reduced leakage through the protective barrier between the blood and brain tissue and increased the density of small vessels.
When the level of IGF-1 was reduced in young mice, and its receptor was removed from the vascular wall of old mice, both improvements weakened. This experiment is called heterochronic parabiosis, where an old and young mouse are surgically connected to share a circulatory system. In a 2024 study, the same group found that old partners had a less permeable blood-brain barrier and a denser network of capillaries, the smallest vessels.
The new study checks which signal in the shared blood is involved in these changes. The authors chose IGF-1, a signaling protein whose level in the blood decreases with age. To respond to it, the protein must enter the shared circulation, and the inner lining of the vessel, the endothelium, must receive the signal through the IGF-1R receptor. The researchers evaluated the state of the barrier by introducing glowing molecules of different sizes into the blood and observing whether they exited the vessels into the brain tissue, as reported in Nature Aging, July 2026.
🔗 Read original →
SpringerLink
Endothelial IGF-1/IGF-1R signaling supports young-blood-induced restoration of blood–brain barrier integrity and microvascular…
GeroScience - Aging is associated with blood–brain barrier (BBB) breakdown and microvascular rarefaction, key contributors to cerebral neuroinflammation, hypoperfusion, and vascular cognitive...
IGF-1 Key to Brain Barrier
The protein IGF-1 has been found to be a crucial link in restoring the protective barrier of the brain in old mice with young circulation. In a study published on August 20, 2026, 18-month-old mice were surgically connected to 4.5-month-old mice through a shared circulatory system. The young circulation reduced leakage through the protective barrier between the blood and brain tissue and increased the density of small vessels.
When the level of IGF-1 was reduced in young mice, and its receptor was removed from the vascular wall in old mice, both improvements weakened. This type of experiment is called heterochronic parabiosis, where an old and young mouse are surgically connected to share a circulatory system. In a 2024 study, the same group had already found that old partners had a less permeable blood-brain barrier and a denser network of capillaries, the smallest vessels.
The new study checks which signal in the shared blood is involved in these changes. The authors chose IGF-1, a signaling protein whose level in the blood decreases with age. To respond to it, the protein must enter the shared circulation, and the inner lining of the vessel, the endothelium, must receive the signal through the IGF-1R receptor. In one group, IGF-1R was removed from the endothelium of the old mouse, and in another, IGF-1 production was reduced in the liver of the young partner. These interventions test different parts of the same chain. The state of the barrier was assessed through a transparent window in the skull: fluorescent molecules of different sizes were introduced into the blood, and it was observed whether they exited the vessels into the brain tissue. With a deficiency of IGF-1 or its receptor, the smallest of these molecules exited more strongly; the density of capillaries with a diameter of up to 10 micrometers also decreased. In groups with altered IGF-1 or its receptor, part of the improvements were still preserved, as reported in Nature Aging, July 2026.
🔗 Read original →
The protein IGF-1 has been found to be a crucial link in restoring the protective barrier of the brain in old mice with young circulation. In a study published on August 20, 2026, 18-month-old mice were surgically connected to 4.5-month-old mice through a shared circulatory system. The young circulation reduced leakage through the protective barrier between the blood and brain tissue and increased the density of small vessels.
When the level of IGF-1 was reduced in young mice, and its receptor was removed from the vascular wall in old mice, both improvements weakened. This type of experiment is called heterochronic parabiosis, where an old and young mouse are surgically connected to share a circulatory system. In a 2024 study, the same group had already found that old partners had a less permeable blood-brain barrier and a denser network of capillaries, the smallest vessels.
The new study checks which signal in the shared blood is involved in these changes. The authors chose IGF-1, a signaling protein whose level in the blood decreases with age. To respond to it, the protein must enter the shared circulation, and the inner lining of the vessel, the endothelium, must receive the signal through the IGF-1R receptor. In one group, IGF-1R was removed from the endothelium of the old mouse, and in another, IGF-1 production was reduced in the liver of the young partner. These interventions test different parts of the same chain. The state of the barrier was assessed through a transparent window in the skull: fluorescent molecules of different sizes were introduced into the blood, and it was observed whether they exited the vessels into the brain tissue. With a deficiency of IGF-1 or its receptor, the smallest of these molecules exited more strongly; the density of capillaries with a diameter of up to 10 micrometers also decreased. In groups with altered IGF-1 or its receptor, part of the improvements were still preserved, as reported in Nature Aging, July 2026.
🔗 Read original →
SpringerLink
Endothelial IGF-1/IGF-1R signaling supports young-blood-induced restoration of blood–brain barrier integrity and microvascular…
GeroScience - Aging is associated with blood–brain barrier (BBB) breakdown and microvascular rarefaction, key contributors to cerebral neuroinflammation, hypoperfusion, and vascular cognitive...
Longer Lives in Worms
Researchers from McGill University published a study on August 20 in eLife examining nine long-lived lines of the roundworm Caenorhabditis elegans. All of these lines lived longer than typical worms, but in two groups, some of the shared genes worked in opposite directions. The authors then tested some of these genes in experiments on the animals themselves.
The study's authors first confirmed that all nine lines indeed lived longer than typical worms, and then compared them in a single design. For each line, they took at least six independent samples, and for control worms, 18. They measured gene function using RNA-seq, a method that counts RNA and shows how actively a cell is using each gene. The profiles were divided into three groups, with 507 genes showing increased activity in four lines, and 188 of those same genes showing decreased activity in two lines.
The authors checked whether such changes were involved in life extension, rather than just accompanying it. Out of 196 genes active in at least six lines, they were able to test 116 using RNA interference, a method that reduces the activity of a chosen gene. Most interventions did not change lifespan, but seven candidates passed a repeat test, with suppression of each reducing life in both normal worms and a line with disrupted mitochondrial function.
🔗 Read original →
Researchers from McGill University published a study on August 20 in eLife examining nine long-lived lines of the roundworm Caenorhabditis elegans. All of these lines lived longer than typical worms, but in two groups, some of the shared genes worked in opposite directions. The authors then tested some of these genes in experiments on the animals themselves.
The study's authors first confirmed that all nine lines indeed lived longer than typical worms, and then compared them in a single design. For each line, they took at least six independent samples, and for control worms, 18. They measured gene function using RNA-seq, a method that counts RNA and shows how actively a cell is using each gene. The profiles were divided into three groups, with 507 genes showing increased activity in four lines, and 188 of those same genes showing decreased activity in two lines.
The authors checked whether such changes were involved in life extension, rather than just accompanying it. Out of 196 genes active in at least six lines, they were able to test 116 using RNA interference, a method that reduces the activity of a chosen gene. Most interventions did not change lifespan, but seven candidates passed a repeat test, with suppression of each reducing life in both normal worms and a line with disrupted mitochondrial function.
🔗 Read original →
PubMed Central (PMC)
Multiple molecular pathways to longevity with opposing gene expression programs defining distinct aging strategies in Caenorhabditis…
While aging is the greatest risk factor for the development of neurodegenerative disease, the role of aging in these diseases is poorly understood. Our previous work has shown that targeting aging pathways can be neuroprotective in animal models of ...
Longer Life in Worms
Researchers from McGill University published a study on August 20 in eLife examining nine long-lived lines of the roundworm Caenorhabditis elegans. All of these lines lived longer than normal worms, but in two groups, some of the same genes worked in opposite directions. The authors then tested some of these genes in animal experiments.
The study found that mutations that extend life are usually studied one line at a time and under different conditions, which can reflect both biology and experimental design. The authors first confirmed that all nine lines indeed lived longer than normal worms, and then compared them in a single design. For each line, they took at least six independent samples, and for control worms, 18 samples.
The authors measured gene function using RNA-seq, a method that counts RNA and shows how actively a cell uses each gene. The profiles were divided into three groups, with 507 genes showing increased activity in four lines, and 188 of the same genes showing decreased activity in two lines. A similar divergence was found in genes regulated by the DAF-16/FOXO protein, which turns other genes on and off.
🔗 Read original →
Researchers from McGill University published a study on August 20 in eLife examining nine long-lived lines of the roundworm Caenorhabditis elegans. All of these lines lived longer than normal worms, but in two groups, some of the same genes worked in opposite directions. The authors then tested some of these genes in animal experiments.
The study found that mutations that extend life are usually studied one line at a time and under different conditions, which can reflect both biology and experimental design. The authors first confirmed that all nine lines indeed lived longer than normal worms, and then compared them in a single design. For each line, they took at least six independent samples, and for control worms, 18 samples.
The authors measured gene function using RNA-seq, a method that counts RNA and shows how actively a cell uses each gene. The profiles were divided into three groups, with 507 genes showing increased activity in four lines, and 188 of the same genes showing decreased activity in two lines. A similar divergence was found in genes regulated by the DAF-16/FOXO protein, which turns other genes on and off.
🔗 Read original →
PubMed Central (PMC)
Multiple molecular pathways to longevity with opposing gene expression programs defining distinct aging strategies in Caenorhabditis…
While aging is the greatest risk factor for the development of neurodegenerative disease, the role of aging in these diseases is poorly understood. Our previous work has shown that targeting aging pathways can be neuroprotective in animal models of ...